Learning objectives.
By reading this article you should be able to:
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Identify the various types of epilepsy surgery available and how the most appropriate procedure is selected.
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Discuss the different types of intraoperative neuromonitoring that may be indicated and the implications for anaesthesia care.
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Work as part of an interdisciplinary team including neurosurgeons and neurophysiologists to optimise outcomes for patients.
Key points.
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Resection of epileptogenic foci can cure epilepsy in certain patients.
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Long-term antiepileptic drugs (AEDs) have adverse effects. These must be screened for before surgery, and their use during the perioperative period should be guided by an epileptologist.
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Anaesthetic agents affect intraoperative electrocorticography in a variable manner.
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Intraoperative seizures may be triggered during pharmacoactivation or functional mapping, and drugs to terminate them should be administered in consultation with the neurophysiologist.
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Slow emergence and postoperative seizures are common and must be anticipated.
Epilepsy is a common chronic neurological condition, with an estimated median incidence of 50.4 per 100,000 persons yr−1, and is characterised by temporary neurological dysfunction manifesting as seizure episodes with focal, generalised or unknown onset.1 Epilepsy increases the annual risk of sudden death to 5.4 times that of matched controls and is also associated with increased morbidity associated with seizures, including injuries from falls and burns.2 Recurrent seizures can result in limitations to participation in education, employment, driving and social activities. In selected patients with epilepsy refractory to medical therapy, surgery represents the best option for curing or significantly improving their seizures. The term ‘epilepsy surgery’ refers to procedures aimed at resecting epileptogenic foci; disconnection surgeries to reduce seizure frequency and propagation; and procedures aimed at reducing seizure frequency via neuromodulation. The provision of anaesthesia care for these surgeries requires a comprehensive understanding of the underlying disease process and a collaborative interdisciplinary approach to intraoperative neuromonitoring.
Aetiology of focal epilepsy
Population studies suggest a predominance of the incidence of focal seizures over generalised seizures.3 A variety of intracranial lesions may act as an epileptogenic focus and may be amenable to surgical resection.
Hippocampal sclerosis
Also known as mesial temporal sclerosis, this condition is characterised by focal neuronal loss and gliosis particularly in the cornu ammonis area 1 and subiculum of the hippocampus. It is the most commonly encountered histopathological finding in epilepsy, identified in 36.4% of all surgical specimens.4 Patients typically experience complex partial seizures with or without aura or progression to generalised tonic–clonic seizures.
Primary brain tumours
Low-grade tumours, particularly gangliogliomas and dysembryoplastic neuroepithelial tumours (DNETs), can be responsible for epilepsy refractory to medical therapy. These are typically slow-growing tumours, and the aims of surgery are to cure the patient's seizure disorder and to ensure a complete surgical resection of the neoplasm if possible. Seizure-free rates of 79% at 5 yrs are reported.5 Long-standing epilepsy, the presence of a remote focus and incomplete tumour removal are associated with worse outcomes.
Malformations of cortical development
Malformations of cortical development represent the most common pathologic finding in children and are characterised by abnormalities in the six layers of the cerebral cortex. Focal cortical dysplasias account for the majority of these malformations, and they are often localised to the frontal lobes. These lesions typically have comparatively less successful outcomes after resection surgery. This may be attributable to an extratemporal location, the presence of multiple lesions and the difficulty locating these malformations on imaging.
Other causes
Vascular malformations can lead to drug-resistant epilepsy, the most common of these being cavernous angiomas of the temporal lobe. Glial scars, which may be the result of previous trauma or stroke, are also responsible for a small minority of cases.6 Encephalitis, usually Rasmussen's encephalitis, is another rare pathological finding. In less than 10% of cases, no specific pathological diagnosis is found on resected specimens.
Selection of patients for surgery
The primary criterion for selection of appropriate patients for any form of epilepsy surgery is a history of chronic seizures that are refractory to medical therapy. A series of investigations to determine their suitability for surgery is performed with MRI imaging, EEGs and a neuropsychological evaluation considered as mandatory investigations for all patients.7 Where an epileptogenic focus is identified, resection surgery may be undertaken. In cases with no identifiable focus, insertion of a seizure modulation device or a disconnection surgery may be an option. Based on the results of the following investigations patients are advised of the likelihood of benefit from surgery and the risks involved. Ultimately the patient needs to decide whether their epilepsy is having an impact on their activities of daily living to such a degree that they are willing to proceed with surgery. They should understand the risks that are involved and the likelihood of benefit.
Imaging
High-resolution MRI (3 Tesla) is the cornerstone of imaging for epilepsy resection surgery as lower resolution scanning may miss the more subtle lesions. In patients who have no positive MRI findings, [18F]-2-deoxyglucose PET (FDG-PET) scanning can be used to assess for areas of impaired glucose metabolism.8 Single-photon emission computed tomography (SPECT) scanning can be used to localise the increased cerebral flow to epileptogenic zones during seizures.9 Postprocessing of SPECT images and coregistering these with MRI images (SISCOM) can improve the sensitivity and specificity of localisation.10
Electroencephalography
In all cases either routine or video EEGs are performed to localise seizures, and this requires admission to an epilepsy monitoring unit. This also allows for examination of the patient during seizure episodes to help with functional localisation. Methods used to provoke seizures include tapering of AEDs, sleep deprivation, hyperventilation and photic stimulation.
Localisation of speech and language centres
Some patients will require localisation of their speech and language function in order to determine the limits of their resection surgery and their likely postoperative speech and memory function, for example in the case of a left temporal or parietal lesion. Traditionally this has been investigated using the intracarotid amobarbital test, also known as the Wada test, in which a catheter is placed into one of the internal carotid arteries, and memory and language function are tested after the injection of an anaesthetic agent. Propofol, etomidate, pentobarbital and methohexital can all be used as alternatives to amobarbital and occasionally the presence of an anaesthetist may be requested for these tests. Increasingly, functional MRI is used to localise speech and memory functions and may be a more sensitive tool than the Wada test.11
Neuropsychological assessment
Neuropsychological assessment can help to localise seizure foci and to advise patients of their likely postoperative memory function post resection. Epilepsy is more common among people with intellectual disabilities and these patients can be particularly challenging to manage during the perioperative period.12
Invasive EEG monitoring
In order to localise epileptogenic foci, some patients will require the placement of intracranial electrodes for long-term monitoring (generally 1–2 weeks). Subdural strips or grids can be placed on the surface of the brain via a mini or standard craniotomy depending on the area of interest (Fig. 1). Stereoelectroencephalography (SSEG) refers to the insertion of depth electrodes into targeted areas of the brain parenchyma. This allows for EEG examination of deeper brain structures. Depth electrodes can be inserted via a burrhole. Commonly subdural grids and depth electrodes are inserted together to improve accuracy of localisation. SSEG has a morbidity rate of 9.1% including complications of haematoma formation, infection and cerebral oedema.13 Despite this morbidity the overall yield for successful localisation of epileptogenic foci from these procedures remains high.14
Fig 1.
An 8×8 cm subdural electrode grid placed for long-term EEG monitoring.
Children undergoing invasive EEG monitoring (IM) will require one-to-one nursing care for at least 24 h. Adequate postoperative analgesia must be given in order to minimise agitation. An agreed plan must be in place with the epilepsy team regarding the management of focal and generalised seizures during this time. In general, children will have IM for shorter periods compared with adults, and an early return to the operating theatre for removal of monitoring with or without resection surgery should be planned.
Types of epilepsy surgery
Temporal resection
Resection of the anterior temporal pole, the amygdala and part of the hippocampus is the most commonly performed epilepsy resection surgery. In patients who have temporal lobe epilepsy, typically the posterior margin of the resection is 4.0–4.5 cm back from the temporal pole on the dominant side and 5.0–5.5 cm on the non-dominant side, in order to minimise impact on the language centre and visual radiations. This procedure results in a significant reduction in seizure activity compared with standard medical therapy.15 Approximately 25% of patients will develop a degree of memory impairment after temporal lobectomy. Less common are visual field defects caused by damage to the inferior optic radiations.
Extratemporal resection
Focal lesion, lobar or multilobar resections can be undertaken in the frontal, occipital and parietal lobes with the expectation of curing or improving seizures. Lesions in eloquent areas of speech, language and motor function may not be suitable for resection given the postoperative implications of this procedure. In areas adjacent to motor and somatosensory cortex, intraoperative neuromonitoring may be required (see below). The outcomes from non-lesional or MRI-negative resections are less successful.
Hemispherectomy
Hemispherectomies are usually undertaken in children who have diffuse disease pathology primarily affecting one cerebral hemisphere (Fig. 2). The aetiology of such disease includes perinatal stroke, Sturge–Weber syndrome, Rasmussen's encephalitis, hemimegalencephaly and multilobar cortical dysplasia. In an anatomic hemispherectomy the frontal, parietal, temporal and occipital lobes are removed with the basal ganglia and thalamus left in place. Functional hemispherectomies involve the removal of a smaller amount of the affected hemisphere and complete disconnection to the opposite hemisphere. The large craniotomy required with ligations of the anterior and middle cerebral arteries mean that hemispherectomies can result in large volume blood loss. Despite the risk, seizure-free rates of 60–90% are reported after hemispherectomies, with better predicted outcomes where the aetiology is stroke or Sturge–Weber syndrome compared with malformations of cortical development; as the latter are likely to have a greater crossover effect to the contralateral hemisphere.16
Fig 2.
T2 MRI image from a 12-year-old patient who had a subtotal hemispherectomy for hemimegalencephaly at 23 months of age. Having been seizure-free for a number of years, the patient began having focal seizures arising from residual left occipital lobe. The red arrow indicates a gliotic left occipital lobe. The patient subsequently underwent a successful resection of this residual occipital lobe tissue.
Laser interstitial thermal therapy
This is an emerging, less invasive technology involving the introduction of a fibreoptic catheter via a burrhole for the MRI-guided laser ablation of selected epileptogenic foci, most commonly in the temporal lobe. Patients require a GA either in the operating theatre with subsequent transfer to the MRI suite or with some systems the entire procedure can be undertaken in the MRI suite. Laser interstitial thermal therapy (LITT) is associated with quicker hospital discharge and less postoperative pain and memory loss.17
Disconnection surgery
The corpus callosum is the largest white matter tract in the body, connecting the two cerebral hemispheres. In refractory generalised or multifocal epilepsy the corpus callosum can be transected, either the anterior two thirds or a complete corpus callostomy. This is particularly indicated in patients who experience drop attacks. Total corpus callostomy results in a higher rate of seizure reduction compared to anterior corpus callostomy, but it is also associated with a higher rate of disconnection syndrome.18
Functional hemispherotomy disconnects entirely the pathologic from the healthy cerebral hemisphere. In patients with infantile hemiplegic epilepsy this may provide the safer option for seizure reduction with less of the risks incurred with undertaking a hemispherectomy. The aims of a complete functional hemispherotomy are: disconnection of the corticothalamic tract; resection of the medial temporal structures; a total corpus callosotomy; and disconnection of the orbitofrontohypothalamic tract.16
Seizure modulation devices
Vagal nerve stimulation (VNS) has been approved in Europe for the treatment of drug-resistant epilepsy since 1994. The exact mechanism of action remains unclear. More than 60% of patients will have at least a 50% reduction in seizure burden with long-term VNS therapy.19 Although right vagus nerve stimulation is possible, because of the predominant innervation of the right vagus nerve to the sinoatrial node, devices are routinely implanted onto the left vagus nerve in the cervical region. Because the vagus nerve is located between the internal carotid artery and internal jugular vein, large volume blood loss is a risk during implantation and explantation, but it is not widely reported. A single lead forms three helical coils which are wrapped around the nerve. During lead impedance testing there is a small risk of bradycardia and asystole.20
Deep brain stimulation (DBS) is another option in patients with treatment resistant epilepsy who are unsuitable for resection surgery. The mechanism of action of this treatment modality is incompletely understood but may involve reducing neuronal activity in the target area.21 Common target sites for implantation of electrodes include the thalamic nuclei, hippocampus, subthalamic nucleus and cerebellum. Generators are typically implanted below the clavicle but can also be placed intracranially. Classically DBS refers to ongoing stimulation to prevent the onset of seizures. Responsive stimulation refers to stimulation that is delivered only when a seizure is about to begin.
Conduct of anaesthesia
Preoperative management
Preoperative assessment is preferably done in a preanaesthesia clinic. Usually patients will be prescribed a selection of AEDs which should be taken as usual on the day of surgery. An exception may be if electrocorticography is being used, in which case the epileptologist may then advise that the patient does not take some or all of their regular medications. Dysnatraemias, thrombocytopenias, leucopenias and deranged liver function tests are adverse effects from long-term use of AEDs, and a full blood count, renal profile and liver function tests should be checked before surgery. Table 1 lists the characteristics of some AEDs, and these have been discussed in more depth in this journal.22 An electrocardiogram should be routinely performed given the common finding of Brugada-type ST changes and J wave abnormalities that are often associated with sodium channel blocking AEDs. Outlining the nature of the patient's regular seizure type (e.g. presence of aura, automatisms) will aid in recognition of seizure activity after surgery.
Table 1.
Characteristics of the most common anti-epileptic drugs (AEDs) classified as per their primary mode of action. CYP, cytochrome 450; UGTs, metabolism by uridine 5′ diphosphate glucuronyltransferases; P-gp, membrane P-glycoprotein multidrug resistance transporter; LFTs, liver function tests; GABA, gamma aminobutyric acid
| Mechanism of action | Drug | Effect on drug metabolism | Adverse effects |
|---|---|---|---|
| Sodium channel effects | Carbamazepine | Potent CY2P, UGT and P-gp inducer | Hyponatraemia, leucopenia, cardiac conduction abnormalities |
| Eslicarbazepine | Mixed inducer and inhibitor | Hyponatraemia, increased PR interval, deranged LFTs | |
| Oxcarbazepine | Mixed inducer and inhibitor | Hyponatraemia, rare cause of Steven–Johnson syndrome | |
| Phenytoin | Potent CY2P and UGT-glucuronidation inducer | Rash, gingival hypertrophy, decreased bone density | |
| Lacosamide | Minor CYP2C19 inhibitor | PR prolongation, potential interaction with other AEDs | |
| Zonisamide | None | Weak carbonic anhydrase inhibitor, nephrolithiasis, cognitive and psychiatric adverse effects | |
| Lamotrigine | Minor inducer of own metabolism (UGT) | Somnolence, rash, hypersensitivity reactions, aseptic meningitis | |
| Modulation of GABA activity | Clobazam | Moderate inhibitor CYP2D6 | Somnolence, dysarthria, mood changes |
| Phenobarbital | Potent enzyme inducer | Osteomalacia, Dupuytren's contracture, megaloblastic anaemia (rare) | |
| Glutamate receptor blockade | Perampanel | None significant but can affect hormonal contraceptives | Neuropsychiatric effects |
| Calcium channel blockade | Ethosuximide | None | Nausea, vomiting, sleep disturbance |
| Multiple mechanisms of action | Valproate | Mixed inhibitor and inducer CYP group | Metabolic syndrome, thrombocytopenia, coagulation disorders, hepatotoxicity |
| Topirimate | Minor CYP3A4 inducer, minor CYP2C19 inhibitor | Weight loss, paraesthesia, metabolic acidosis | |
| Primidone | Potent enzyme inducer | Osteopenia, QT interval changes, deranged LFTs | |
| Other mechanisms of action | Levetiracetam | None | Neuropsychiatric effects |
| Brivaracetam | Weak inhibitor | Irritability, anxiety, hypersensitivity reactions | |
| Gabapentin | None | Sedation, weight gain | |
| Cannabidiol | Likely moderate inducer CYP450 | Somnolence, vomiting, abnormal LFTs |
Intraoperative management
The core principles of neuroanaesthesia include maintenance of adequate cerebral perfusion pressure and avoidance of increases in intracranial pressure. Nitrous oxide increases cerebral blood volume and possibly cerebral metabolic rate (CMR) and is best avoided. The relationship between inhalation anaesthetic agents and cerebral blood flow is complex, and in most cases an increase in cerebral blood volume is offset by a decrease in CMR. It is a common practice in neuroanaesthesia to use sevoflurane or isoflurane to a level of 1 MAC with a remifentanil infusion for maintenance of anaesthesia. Long-term administration of AEDs is associated with resistance to neuromuscular blocking agents.23 For the most common procedure of anterior temporal lobectomy and most other standard craniotomies, an arterial cannula and large-bore peripheral venous access is sufficient, with central venous catheterisation generally not required. Care should be taken during positioning as excessive rotation of the head may impede cerebral venous drainage. Application of skull clamps or Mayfield pins is extremely stimulating, and depth of anaesthesia should be increased at that time or a short-acting opioid or bolus of propofol given to reduce the surge in arterial pressure that can occur. A remifentanil infusion of 0.1–0.5 μg kg−1 min−1 can be given intraoperatively and decreased when closure of the dura begins with administration of a longer acting opioid for postoperative analgesia. Some patients may be following a ketogenic diet, in which case the use of normal saline solutions is preferable to lactated Ringer's solution. Cross-matched blood should be available for all craniotomies.
Intraoperative electrocorticography
For selected surgeries, a short period of invasive EEG monitoring may be required during surgery: EEG electrodes are placed directly on the cortical surface and epileptiform activity is identified, and this can guide the extent of a resection. This technique is referred to as intraoperative electrocorticography (ECoG). The continuous EEG tracing pattern is referred to as the background ECoG. Interictal epileptiform activities (IEAs) are the spikes, waves and combination EEG patterns that are typically seen in epilepsy in the period between clinical seizures. As the intraoperative time is short, clinical seizures are usually not captured by ECoG, but the presence and location of IEAs can be used to localise the epileptogenic focus and guide the resection. Hippocampography is a specific form of ECoG involving a single strip or depth electrode placed along the ventricular aspect of the hippocampus to guide the extent of mesial temporal resection. Its use is associated with a more consistent hippocampal resection.24
If ECoG is required, then benzodiazepines should not be given on induction because they suppress EEG activity. During ECoG, pharmacoactivation may be required in order to activate IEAs. Potent short-acting μ-agonists can be used to increase IEAs and alfentanil, remifentanil, fentanyl and sufentanil can be used for this. Alfentanil is the most specific and consistent activator of IEAs and is administered at doses of 20–100 μg kg−1 for this purpose.25 It is generally accepted that the depth of anaesthesia should be reduced during ECoG, and the patient should be advised of the small risk of awareness during this period.26 The variable effects of anaesthetic agents on both the background ECoG and on IEAs or spikes are summarised in Table 2. Neuromuscular blockade may be used to prevent movement and interference with ECOG; it should be noted that laudanosine, a metabolite of atracurium and cisatracurium, is potentially epileptogenic.27
Table 2.
Effects of anaesthetic agents on intraoperative electrocorticography (ECoG) and intraictal epileptiform activities (IEAs). MAC, minimum alveolar concentration
| Activates IEAs | Suppresses IEAs | Variable IEA effect | Background ECoG | |
|---|---|---|---|---|
| Intravenous anaesthetics | Thiopental—activation with boluses Etomidate—may provoke seizures Ketamine—non-specific activation Methohexital—significant activation of spikes |
Benzodiazepines | Propofol—may activate or suppress spikes with variable effect over all dose ranges Dexmedetomidine—no evidence of activation or suppression |
An initial desynchronisation is seen followed by progression into β, θ and δ waves and subsequent burst suppression. Benzodiazepines and dexmedetomidine have a similar spectral profile. |
| Inhalation anaesthetics | Sevoflurane—non-specific dose-dependent activation Enflurane—may provoke seizure particularly if Paco2 low |
Halothane Nitrous oxide—suppresses at concentrations >50% and acts synergistically with other agents |
Desflurane—no evidence of activation Isoflurane—may suppress spikes especially if used with nitrous oxide Xenon—effect unclear but likely does not cause activation |
Burst suppression achieved at concentrations >1.5 MAC |
| Opioids | Fentanyl, alfentanil, remifentanil, sufentanil—all cause activation at high doses and potentially at common clinical doses Pethidine—probably causes activation |
Morphine, hydromorphone—likely no effect at clinical doses but potentially at high doses | Low-dose infusions have no effect on background ECoG |
Intraoperative functional neuromonitoring
If the resection area involves or is adjacent to the somatosensory or motor cortex then monitoring of somatosensory evoked potentials (SSEPs) and motor evoked potentials (MEPs) may be required. A TIVA technique is preferable in this case to minimise interference with monitoring.28 If MEPs are monitored then the muscles of mastication will be activated. A reinforced tracheal tube should be used, and care must be taken to place an appropriately sized bite block between the molars ensuring that the tongue and cheeks are free. Direct cortical stimulation with motor mapping is associated with an increased risk of seizures compared to transcranial electrical stimulation alone.
Awake craniotomy
There are two main advantages of resection of epileptogenic foci in the awake patient. Firstly, for lesions in eloquent areas of speech and sensorimotor function, surgery in the awake patient allows for continuous monitoring of these functions, that is language and sensorimotor mapping, to guide the extent of the resection. Secondly, ECoG can be performed without the interference of anaesthetic agents. Disadvantages include a limited surgical time, limited craniotomy incision and the recording of only intraictal episodes by ECoG. Awake craniotomies require a calm and cooperative patient and are often not feasible in children, those with intellectual disabilities or a significant psychiatric history.29
Management of intraoperative seizures
If pharmacoactivation during ECoG or cortical electrical stimulation for functional mapping is required, the patient may develop seizures. These are usually focal seizures that cease when stimulation has stopped, but they may progress to generalised tonic–clonic seizures. The first step in management is to irrigate the surgical field with ice cold saline. If this manoeuvre fails, then propofol boluses of 10–30 mg should be administered. Subsequently benzodiazepines (midazolam 2–5 mg) or thiopental (25–50 mg) can be used if the seizure is ongoing. Management of intraoperative seizures should be in conjunction with the neurophysiologist given that any drug administered for the termination of seizures may affect subsequent ECoG monitoring.
In cases where ECoG is not being used, the detection of seizures is challenging. Younger age, recent seizure activity, frontal and parietal lesions and certain tumours such as oligodendrogliomas are all associated with an increased risk of developing intraoperative seizures.30 Hypocapnia can also provoke seizure activity and should be avoided. Clinical signs include tachycardia, hypercarbia, pupillary dilatation and muscle rigidity. Fluctuations in bispectral index (BIS) are observed with intraoperative seizures, generally seen as a decrease in BIS level followed by an increase. Reports of BIS changes with seizures are inconsistent and in the context of epilepsy surgery can be misleading. If there is a concern regarding seizure activity in the absence of EEG monitoring, the depth of anaesthesia should be increased and a benzodiazepine administered.
Postoperative considerations
Delayed emergence is common in patients after epilepsy surgery for several reasons: associated neurological conditions; use of AEDs; intraoperative seizures and a postictal state; and drugs administered to terminate seizures. Some patients with an ‘irritable’ EEG may require loading doses of AEDs during surgery after recording, or after operation. Administration of large doses of opioids should be avoided and in the absence of large blood loss or other contraindications non-steroidal anti-inflammatory drugs can be given.
As with all neurosurgical cases, there is a risk of development of intracranial haemorrhage after operation. Seizures and the postictal state may cloud neurological assessment and early detection of new haemorrhage. For generalised tonic–clonic seizures occurring in the PACU, benzodiazepines are first-line therapy. Given that seizure activity causes an increase in lactate, the lactate level should not be used in isolation to guide fluid management or as a criterion for discharge from the PACU. It is important that doses of AEDs are not missed after surgery. Given that many AEDs cause hepatic enzyme induction or inhibition, the different interactions should be considered. Enzyme-inducing drugs decrease the serum concentrations of many drugs including paracetamol, fentanyl and some antibiotics, whereas enzyme-inhibiting drugs may increase serum concentrations of antibiotics and in particular other AEDs. Weaning of AEDs after resection surgery should be managed by an epileptologist.
Repeated epilepsy surgery
Repeated epilepsy resection surgeries are common. In some cases the first resection may have been limited because of concerns over postoperative deficits. In other cases patients may have had a seizure-free period of months to years before developing seizures again, potentially because of gliosis formation at the surgical site. The risk of blood loss is increased with second and subsequent craniotomies.
Battery replacement for VNS devices is a quick procedure which can be undertaken as a day case, and in most instances use of a supraglottic airway is sufficient.
Summary
Epilepsy surgery encompasses a broad variety of surgeries, including resections of epileptogenic foci, disconnection surgeries and insertion of neuromodulation devices. The anaesthetist should understand the different types of ECoG and functional neuromonitoring that may be required and be familiar with how various anaesthetic agents can impact this. Good communication between the anaesthetist, neurosurgeon and neurophysiologist is imperative in these cases.
Declaration of interest
The authors declare that they have no conflicts of interest.
MCQs
The associated MCQs (to support CME/CPD activity) will be accessible at www.bjaed.org/cme/home by subscribers to BJA Education.
Biographies
Caroline Larkin MD FCAI FJFICMI MRCPI is a consultant anaesthetist with a special interest in neuroanaesthesia.
Donncha O'Brien FRCSI MD FRCSI (Surg. Neurology) is a consultant neurosurgeon and the national lead for paediatric and adult epilepsy surgery in the Republic of Ireland.
Darshana Maheshwari FCPS, FCAI is a fellow in neuroanaesthesia and neurocritical care.
Matrix codes: 1A02, 2A03, 3F00
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